Ocular infection with herpes simplex virus is the most prevalent severe ocular infection in this country. The propensity of this infection to recur (spontaneously) throughout life and to produce irreversible structural alterations of the cornea and intraocular structures results in considerable visual morbidity, medical expense and loss of productivity in individuals. Clinical management of herpetic keratitis is directed toward control of replicating virus in the cornea and adnexal tissues. To date, there is no method for blocking access of the virus to latency sites, or preventing recurrent shedding of the virus from these sites. The key to control of this disease, and other related herpes virus type infections seems to be in elucidating the mechanism(s) of latency and reactivation. The use of an in vitro model of HSV-1 latency and reactivation in isolated trigeminal ganglion cells offers a defined efficient and easily controlled system for study of mechanisms associated with HSV natural history. This drug induced suppression model, in conjunction with immunofluorescent staining, electrophysiological recording and ultrastructural examination can be used to define and characterize the triggering stimuli responsible for the establishment of latency and reactivation. Through elucidation of these parameters, antiviral treatment directed toward control and eradication of latent viral disease may be enhanced. The development of a compartmentalized model of HSV-1 natural history would provide an ideal means of studying viral transport, sequestering and reactivation at the cellular level. Ionic, electrophysiological, antigenic and morphological characterization of physiological mechanisms associated with virus latency in this system would be applicable to those conditions occuring during in vivo HSV-1 challenge.